Inflammation and Oxidative Stress: The Molecular Connectivity between Insulin Resistance, Obesity, and Alzheimer's Disease.
Inflammation and Oxidative Stress: The Molecular Connectivity between Insulin Resistance, Obesity, and Alzheimer's Disease.
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DOI：
10.1155/2015/105828
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发表时间：
2015
影响因子：
4.6
通讯作者：
Newsholme P
中科院分区：
文献类型：
--
作者：
Verdile G;Keane KN;Cruzat VF;Medic S;Sabale M;Rowles J;Wijesekara N;Martins RN;Fraser PE;Newsholme P
2型糖尿病（T2DM）、阿尔茨海默病（AD）和胰岛素抵抗是与年龄相关的疾病，患病率的增加是公众关注的问题。最近的研究提供的证据表明，胰岛素抵抗和受损的胰岛素信号可能是糖尿病，痴呆症和其他神经系统疾病进展的一个促成因素。阿尔茨海默病（Alzheimer's disease，AD）是痴呆症最常见的亚型。胰岛素释放减少（对于T2DM）和作用降低是T2DM和AD发生和进展的关键。进行文献检索以确定肥胖、糖尿病和AD之间的分子共性。胰岛素抵抗通过受损的胰岛素信号传导或通过血液中葡萄糖和脂质（胆固醇和三酰甘油）代谢和浓度的异常变化影响许多组织和器官。尽管流行病学和生物学证据强调了T2DM患者中认知功能下降和AD的发生率增加，但细胞和组织功能障碍的共同分子基础正在迅速获得认可。作为原因或结果，与T2DM相关的慢性炎症反应和氧化应激、淀粉样β（Aβ）蛋白蓄积和线粒体功能障碍将T2DM和AD联系起来。
Type 2 diabetes (T2DM), Alzheimer's disease (AD), and insulin resistance are age-related conditions and increased prevalence is of public concern. Recent research has provided evidence that insulin resistance and impaired insulin signalling may be a contributory factor to the progression of diabetes, dementia, and other neurological disorders. Alzheimer's disease (AD) is the most common subtype of dementia. Reduced release (for T2DM) and decreased action of insulin are central to the development and progression of both T2DM and AD. A literature search was conducted to identify molecular commonalities between obesity, diabetes, and AD. Insulin resistance affects many tissues and organs, either through impaired insulin signalling or through aberrant changes in both glucose and lipid (cholesterol and triacylglycerol) metabolism and concentrations in the blood. Although epidemiological and biological evidence has highlighted an increased incidence of cognitive decline and AD in patients with T2DM, the common molecular basis of cell and tissue dysfunction is rapidly gaining recognition. As a cause or consequence, the chronic inflammatory response and oxidative stress associated with T2DM, amyloid-β (Aβ) protein accumulation, and mitochondrial dysfunction link T2DM and AD.